scholarly journals Effect of acetyl-l-carnitine on ovarian cancer cells' proliferation, nerve growth factor receptor (Trk-A and p75) expression, and the cytotoxic potential of paclitaxel and carboplatin

2009 ◽  
Vol 112 (3) ◽  
pp. 631-636 ◽  
Author(s):  
David B. Engle ◽  
Jennifer A. Belisle ◽  
Jennifer A.A. Gubbels ◽  
Sarah E. Petrie ◽  
Paul R. Hutson ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Growth Factor Receptor ◽  
Nerve Growth Factor Receptor ◽  
Ovarian Cancer Cells ◽  
Cytotoxic Potential ◽  
Nerve Growth ◽  
Trk A

scholarly journals Nerve Growth Factor Receptor TrkA Signaling in Breast Cancer Cells Involves Ku70 to Prevent Apoptosis

2007 ◽  
Vol 6 (11) ◽  
pp. 1842-1854 ◽  
Author(s):  
Emmanuelle Com ◽  
Chann Lagadec ◽  
Adeline Page ◽  
Ikram El Yazidi-Belkoura ◽  
Christian Slomianny ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Growth Factor Receptor ◽  
Nerve Growth Factor Receptor ◽  
Nerve Growth

scholarly journals Nerve growth factor receptor negates the tumor suppressor p53 as a feedback regulator

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Xiang Zhou ◽  
Qian Hao ◽  
Peng Liao ◽  
Shiwen Luo ◽  
Minhong Zhang ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Dna Binding ◽  
Cancer Cells ◽  
Human Cancer ◽  
Growth Factor Receptor ◽  
Chemotherapeutic Agents ◽  
Nerve Growth Factor Receptor ◽  
Breast Cancers ◽  
Nerve Growth

Cancer develops and progresses often by inactivating p53. Here, we unveil nerve growth factor receptor (NGFR, p75NTR or CD271) as a novel p53 inactivator. p53 activates NGFR transcription, whereas NGFR inactivates p53 by promoting its MDM2-mediated ubiquitin-dependent proteolysis and by directly binding to its central DNA binding domain and preventing its DNA-binding activity. Inversely, NGFR ablation activates p53, consequently inducing apoptosis, attenuating survival, and reducing clonogenic capability of cancer cells, as well as sensitizing human cancer cells to chemotherapeutic agents that induce p53 and suppressing mouse xenograft tumor growth. NGFR is highly expressed in human glioblastomas, and its gene is often amplified in breast cancers with wild type p53. Altogether, our results demonstrate that cancers hijack NGFR as an oncogenic inhibitor of p53.

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